Hypothalamic Pituitary Relationships and Biofeedback Pt. 1 Flashcards

(33 cards)

1
Q

Describe the parts and structure of the pituitary gland

A

Anterior (epithelial/adenohypophysis)
Posterior (neural/neurohypophysis)
Hypophyseal stalk connects it to hypothalamus

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2
Q

What is the first structure affected by a pituitary tumor? Why?

A

Vision as it puts pressure on the optic nerves

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3
Q

What are the features of the posterior pituitary?

A

Neural. Axons extending into the gland and releases hormones (ADH and oxytocin)

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4
Q

What nuclei control the posterior pituitary?

A

SON (supraoptic) and PVN (paraventricular)

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5
Q

What are the features of the anterior pituitary?

A
  • Neural and hormonal connections (connected to hypothalamus via the hypothalamic-hypophyseal blood vessels)
  • release FLAT PG
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6
Q

Describe how the anterior pituitary communicate via hypothalamic-hypophyseal portal system

A

Hormones are released in high concentrations to tropic cells in AP > AP releases hormones in circulation
-Rapid response = prevents buildup of hormones in the circulation

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7
Q

3 families of hormones of the AP
Corticotrophs
Gonadotrophs
Somatotrophs/lactotrophs

A
  • ACTH (stimulated by CRH)
  • TSH/FSH/LH (stimulated by GnRH)
  • GH/Pro (stimulated by GHRH, TRH)
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8
Q

Which hormones have inhibitory mechanisms of action?

A

GHIH (somatostatin) - prevents GH release by somatotrophs

PIF (dopamine) - prevents prolactin release by lactotrophs

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9
Q

What does primary, secondary and tertiary disorder mean?

A

Primary - problem level of the peripheral gland
Secondary - problem level of the pituitary gland
Tertiary - problem level of the hypothalamus

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10
Q

Draw the HPG (hypothalamus-pituitary-gonad axis)

A

Ok

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11
Q

Regulation and action of the FSH and LH hormones

A

Regulated by the pulsatile release of GnRH (fueled by enough body energy). They promote spermatogenesis and estrogen/progesterone/testosterone release

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12
Q

Acromegaly
Cause
Clinical

A
  • Increased exposure to growth hormone due to pituitary adenoma after puberty after the epiphyseal plates have closed
  • growth of extra bone/soft tissue/cartilage growth
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13
Q

Draw the growth hormone axis

A

Ok

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14
Q

What type of signaling does the GH receptor use?

A

JAK-STAT

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15
Q

At what physiological state is the growth hormone usually secreted?

A

Times of hunger/hypoglycemia

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16
Q

What are the actions of GH as it binds directly to MSK?

A

Hypertrophy of cells
Hyperplasia (make more cells)
Increase metabolism

17
Q

How does GH indirectly cause growth?

A

Stimulates the liver to produce IGF-1 which encourages growth of everythingmajority of its effects are done indirectly

18
Q

What happens if there is insensitivity of receptors to growth hormone (primary)?

A

-High GH in circulation and low IGF-1 production in liver

19
Q

What happens when there is secondary (pituitary level deficiency?)
How would you treat this?

A
Pituitary isn't making the GH and liver isn't making IGF-1. High GHRH
GH replacement (Somatropin, Somatrem, Mecasermin)
20
Q

What happens in tertiary (hypothalamic level) deficiency?

How would you treat this?

A

No release of GHRH from the hypothalamus. Low everything.

Semorelin

21
Q

Gigantism
Cause
Clinical

A

Exposure to excess GH due to pituitary adenoma before epiphyseal plates close (before puberty)
-giant

22
Q

How is the HPG axis working during the fed state (favrable)

A

Adequate insulin and amino acid availability. Liver produces IGF-1 > trigger growth processes

23
Q

How is the HPG axis altered in unbalanced fed state (high carbs low protein)

A

High insulin but low AA availability. Can’t make GH, can’t make IGF-1

24
Q

How is HPG axis altered in unbalanced fed state (low carbs high protein)?

A

IGF-1 produced and triggers growth. Inadequate sugar = use fat as energy and result in lipolysis.
Since sugar is low - stimulate gluconeogenesis and increase blood sugar levels

25
How do you diagnoses someone with excess GH (gigantism/acromegaly?
Serum has elevated GH and IGF-1 and fail the oral glucose test (no decrease of GH after oral glucose) Also pituitary enlargement (adenoma)
26
Describe the fluctuation of GH secretion throughout the day
Spike during sleep. During waking hours highest while exercising.
27
What causes stimulation of prolactin secretion?
``` Pregnancy (via estrogen) Breast feeding (suckling) Sleep Stress TRH ```
28
What are pituitary adenomas?
Adenomas release extra hormone and release into bloodstream | Result in hyperpituitarism (prolactinoma)
29
What does the posterior pituitary release?
Oxytocin and ADH (neuropeptides)
30
In the posterior pituitary, what nuclei controls ADH and Oxytocin?
``` ADH = supraoptic nuclei Oxytocin = paraventricular nuclei ```
31
Draw the oxytocin axis
Ok
32
How does Oxytocin stimulate milk ejection?
Contracts the myoepithelial cells lining milk ducts (stimulated by suckling mostly)
33
How does oxytocin stimulate uterine contraction?
Dilation stimulates oxytocin release which stimulates contractions and further dilations. Pitocin induces labor.